Key result
Precision therapies targeting metabolism, mitochondrial dysfunction, and inflammation reshape diverse heart failure management.
Why the study?
Heart failure remains associated with high illness rates and mortality, and effective treatment, particularly for HFpEF, remains limited.
This narrative review synthesizes recent discoveries in the molecular mechanisms of heart failure, highlighting how pathways like inflammation, mitochondrial dysfunction, and fibrosis can inform precision medicine and novel therapeutic targets.
Warrants no practice change for HF phenotypes; leaves open validation of precision targets in prospective trials.
Heart failure (HF) is a major global health problem associated with high illness rates, mortality, and healthcare costs. Although advances in diagnosis and therapy have improved outcomes for some patients, effective treatment-especially for HF with preserved ejection fraction (HFpEF)-remains limited. HF develops through complex interactions among neurohormonal activation, metabolic remodeling, mitochondrial dysfunction, inflammation, fibrosis, and microvascular impairment. Recent discoveries in these areas have revealed new molecular and cellular targets that may lead to more precise therapies. Novel pharmacological agents, metabolic modulators, device-based interventions, and regenerative approaches are reshaping the treatment landscape. In addition, personalized strategies such as multi-omics profiling, biomarker-guided management, and artificial intelligence-assisted diagnosis hold promise for better risk prediction and individualized care. However, translating mechanistic discoveries into clinical benefit remains a challenge. Future research integrating molecular insights with clinical phenotyping will be essential to achieve precision treatment and improved outcomes in patients with HF.
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Zhang et al. (2025) conducted a review in Heart failure. Emerging precision therapeutic strategies targeting metabolic dysregulation, mitochondrial dysfunction, and inflammation are reshaping the treatment landscape for diverse heart failure phenotypes.
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